In recent years, increases have been observed in blood uric acid levels accompanying the Westernization of the diet and overnutrition. There is therefore concern over increases in the occurrence of gout caused by asymptomatic hyperuricemia. Purine bases, purine nucleosides, purine nucleotides and high molecular weight nucleic acids in the diet are digested and absorbed in the digestive tract, and are decomposed into uric acid by the purine decomposing system in the liver. There are numerous epidemiological findings that indicate that ingestion of a diet having a high content of purine compounds is the cause of hyperuricemia and gout. Decreasing an amount of purine compounds ingested is therefore considered to be the most important means for preventing hyperuricemia or gout.
Examples of foods containing large amounts of purine compounds include meat, soft roe, fish eggs and liver. However alcoholic beverages, and particularly beer, also have a considerably high content of purine compounds. In actuality, Kaneko (Kiyoko Kaneko; Nippon Rinsho, 49: 1108-1115 (1991)) conducted a comparison of the purine compound contents of various alcoholic beverages. It was reported that fermented alcoholic beverages such as beer, sake and wine have a higher purine compound content than distilled alcoholic beverages such as whiskey and Shochu, and that beer has the highest purine compound content among fermented alcoholic beverages. Fujimori, et al. reported that a total of 50 to 70 mg/liter of purine compounds are contained in beer (Fujimori, et al., Nyosan, Vol. 9, No. 2, pp. 128-133).
Furthermore, this value was determined by hydrolyzing the purine compounds contained in beer into purine bases with perchloric acid, and then measuring the resulting purine bases with high-performance liquid chromatography.
Although the purine compound content in beer is within the range of 1/100 to 1/10 that of the above-mentioned meat, eggs and liver, since beer is consumed in large amounts, it should be considered to present a greater risk of morbidity for hyperuricemia and gout than distilled alcoholic beverages. Tofler and Woodings (O. B. Tofler and T. L. Woodings; Med. J. Aust. 2, 479-481 (1981)) conducted a 13-year study by grouping subjects into study groups according to the amount of beer consumption, and pointed out the existence of a correlation between the amount of beer consumed and the incidence of gout. Thus, according to the findings of epidemiological studies, beer is currently regarded as presenting the highest risk of morbidity for hyperuricemia and gout among alcoholic beverages.